Evidence map›Paper›PMID 31399589›Full record

ArticleNature communications2019

A STAT3-based gene signature stratifies glioma patients for targeted therapy.

Melanie Si Yan Tan, Edwin Sandanaraj, Yuk Kien Chong, See Wee Lim, Lynnette Wei Hsien Koh, Wai Hoe Ng, Nguan Soon Tan, Patrick Tan, Beng Ti Ang, Carol Tang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 113 citations in OpenAlex.

  1. STAT3 signaling inhibitors for cancer treatment.Trends in pharmacological sciences · 2026
    Review
  2. The CHI3L1 protein plays role as a protecting factor against autophagy in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2026
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Melanie Si Yan TanNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore.ORCID http://orcid.org/0000-0001-6660-5924
Edwin SandanarajNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore.ORCID http://orcid.org/0000-0002-8469-2563
Yuk Kien ChongNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore.
See Wee LimNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore.
Lynnette Wei Hsien KohNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore.
Wai Hoe NgDepartment of Neurosurgery, National Neuroscience Institute, Singapore, Singapore.
Nguan Soon TanSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.ORCID http://orcid.org/0000-0003-0136-7341
Patrick TanDuke-National University of Singapore Medical School, Singapore, Singapore.
Beng Ti AngSingapore Institute for Clinical Sciences, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore. ang.beng.ti@singhealth.com.sg.
Carol TangNeuro-Oncology Research Laboratory, Department of Research, National Neuroscience Institute, Singapore, Singapore. carol_tang@nni.com.sg.
Agency for Science, Technology and Research · SGNational University of Singapore · SGNanyang Technological University · SGNational Neuroscience Institute · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intratumoral heterogeneity is a hallmark of glioblastoma (GBM) tumors, thought to negatively influence therapeutic outcome. Previous studies showed that mesenchymal tumors have a worse outcome than the proneural subtype. Here we focus on STAT3 as its activation precedes the proneural-mesenchymal transition. We first establish a STAT3 gene signature that stratifies GBM patients into STAT3-high and -low cohorts. STAT3 inhibitor treatment selectively mitigates STAT3-high cell viability and tumorigenicity in orthotopic mouse xenograft models. We show the mechanism underlying resistance in STAT3-low cells by combining STAT3 signature analysis with kinome screen data on STAT3 inhibitor-treated cells. This allows us to draw connections between kinases affected by STAT3 inhibitors, their associated transcription factors and target genes. We demonstrate that dual inhibition of IGF-1R and STAT3 sensitizes STAT3-low cells and improves survival in mice. Our study underscores the importance of serially profiling tumors so as to accurately target individuals who may demonstrate molecular subtype switching.

Indexed as

AnimalsCell SurvivalDisease Models, AnimalDose-Response Relationship, DrugDrug SynergismGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenetic Predisposition to DiseaseGlioblastomaHumansImidazolesInsulin-Like Growth Factor Binding Protein 2MicePyrazinesPyrazoles3-(8-amino-1-(2-phenylquinolin-7-yl)imidazo(1,5-a)pyrazin-3-yl)-1-methylcyclobutanolAZD 1480ImidazolesInsulin-Like Growth Factor Binding Protein 2PyrazinesPyrazolesPyrimidinesReceptor, IGF Type 1STAT3 Transcription FactorTemozolomide

Identifiers

PMID31399589
PMCPMC6689009
OpenAlexW2967135265

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.